Resistance to dermatophyte fungi depends on both non-specific and specific immunological mechanisms. Amongst the former epidermal proliferation, unsaturated transferrin and fatty acids in sebum play major roles. In addition activated phagocytic cells destroy dermatophyte fungi in vitro both intra- and extra-cellularly. In experimental murine dermatophytosis immunity is transferred to naive animals with lymphocytes bearing the Thy-1, 2 phenotype. In man after experimental dermatophyte infection there is evidence that activation of T cell mediated immune responses correlates with recovery. By contrast in certain common dermatophyte infections in man there is evidence of poor T lymphocyte mediated responses (lymphocyte blastogenesis, DTH) to specific fungal antigens. An extracellularly expressed inhibitory factor produced by Trichophyton rubrum and other dermatophytes can suppress B and T lymphocyte blastogenesis in vitro. Circulating dermatophyte antigen is present in serum of infected patients and there is evidence of failure of expression of certain activation markers such as ICAM-1 on keratinocytes from chronically infected patients. These findings suggest that immunomodulation due to the presence of factor(s) derived from dermatophytes may play a role in determining the course of infection in some patients.

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Candida albicans is a pathogen of mucosal surfaces but can also cause systemic disease. Its evolution into a commensal and frequent pathogen of humans and animals progressed as the organism developed specific traits which allowed it to survive in a host. One can only speculate as to which traits promoted its survival; however, it would seem that recognition and colonization of host cells would afford a selective advantage over those organisms which could not adhere. Also, colonization could permit egress of the organism into tissues and, with that, escape from the competitive microbial ecology of mucosal surfaces. Recognition of host cells by C. albicans has been the focus of study by a number of investigators. Based upon a number of observations by several research groups, the recognition process appears complex and dependent upon the type of host cell studied. The C. albicans adhesins are cell surface macromolecules, one adhesin resembling the “integrin” receptors of mammalian cells. Based upon functional activity and the type of host cell molecule recognized by the organism, five adhesin systems have been described. Four of these adhesins are mannoprotein or mannan, while the fifth is thought to be chitin. The host cell ligand is either carbohydrate (fucosyl or glucosamine glycosides) or protein (arginine-glycine-aspartic acid, RGD peptide), depending upon the type of host cell, i. e., either epithelial or endothelial. The study of the Candida adhesins is now beginning to shift from its descriptive beginnings to molecular approaches with the ultimate intent of establishing the role of these molecules in virulence.

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The etiological agent of Kawasaki disease is still unknown, but one characteristic change of this disease is arteritis found in coronary arteries, and many cases of this change occur with thrombotic occlusive aneurysm histopathologically. It is therefore believed that in patients the earliest possible prevention of coronary arteritis in the early stage is desirable. The effect of gamma-globulin therapy has thus attracted special interest recently.
Here, we studied the effect of gamma-globulin on the incidence of arteritis in our animal model. The results confirmed that gamma-globulin decreases to induce arteritis (20%) as compared to untreated control (45%). This result was the same as found in groups treated with drugs such as aspirin or predonine.

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A hospital environment was examined for the presence of dermatophytes. A specimen was collected with cellophane adhesive tape and cultured in Actidione and chloramphenicol added peptone-glucose agar plate medium. A total of 110 colonies of dermatophytes was isolated from outpatient slippers, bathmats in the hydrotherapy dressing room and the floor and bathmats in the ward bathroom: 98 (89.9%) colonies of Trichophyton mentagrophytes, 6 (5.5%) colonies of Trichophyton rubrum, 5 (4.6%) colonies of Microsporum canis and 1 (0.9%) colony of Trichophyton sp. An examination using the quotient of the number of colonies isolated to the number of plates as a parameter revealed that the bathmats in the hydrotherapy dressing room and both the floor and mats in the ward bathroom were heavily contaminated with dermatophytes.
Tinea pedis appeared to develop during the inpatient rehabilitation course of 11 patients hospitalized between January 1986 and December 1990. The possibility of nosocomial infection by dermatophytes was investigated. The period between the start of the rehabilitation program and the onset of tinea pedis varied in these patients from 7 to 120 days, averaging 45.9 days. The underlyng disease was cerebrovascular disorder in 3 patients and orthopedic disorder in 8. Further classification was made by dermatophyte species: 7 patients had T. mentagrophytes, 1 had T. rubrum and 2 had mixed infection with T. mentagrophytes and T. rubrum. In the remaining 1 patient, species was unknown. These findings suggest that T. mentagrophytes which is isolated at a relatively high frequency in communal environments could be a source of infection.

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Statistical analysis was performed on 4, 695 patients suffering from dermatophytosis, which represents 7.1% of my outpatient population during the period 1982 to 1991. Sex ratio (male/fe-male) was 1.5:1, and the largest population was individuals in their 4th decade. Among 5, 580 cases of dermatophytoses, tinea pedis was the most frequent (64.0%), followed by teinea unguium (14.2%), tinea cruris (10.4%), tinea corporis (8.2%), tinea manuum (2.8%), tinea capitis (0.3%), kerion celsi (2 cases) and tinea barbae (1 case). The incidence of tinea pedis increased, whereas that of tinea cruris and tinea corporis decreased during the 10 year survey. Thirty point seven % of dermatophytosis cases had two or more clinical types; for example, 81.4% of tinea unguium and 69.2% of tinea manuum cases had concomitant tinea pedis, respectively. 3, 669 dermatophyte fungi were isolated during the survey. They were Trichophyton rubrum (TR) (67.8%), T. mentagrophytes (TM) (26.5%), Microsporum canis (MC) (3.9%), Epidermophyton floccosum (1.6%), M. gypseum (0.1%) and T. violaceum (0.1%).
Sixty three point five % of the dermatophytes isolated from tinea pedis was TR. Among the 144 MC isolated, 120 were from tinea corporis, 15 from tinea capitis, 8 from tinea pedis and 1 was from tinea manuum.
TR was 2.6 times more frequent than TM. This ratio is higher than that of previous reports from Hokkaido prefecture, Japan.

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We have previously shown the importance of the determinant of antigen 6 in the adherence of Candida albicans serotype A (C. albicans A) to epithelial cells using a human mouth squamous cell line as a target. In this study, we investigated the adherance of C. albicans A to epithelial cells other than buccal cells to generalize the role of the antigen 6 determinant in the adherence; three antigenic mutants of C. albicans A were used, which had lost the reactivity with a monoclonal antibody against antigen 6 (MAb-6), and their spontaneous revertants. The adhesive ability of these mutants to all types of epithelial cells used was shown to be markedly lower than that of the parent, while the adhesive ability of the revertants which partially recovered agglutinability with MAb-6 was intermediate between those of the parent and the mutants. On the other hand, strains of C. albicans serotype B, C. stellatoidea, and C. guilliermondii, all of which lack the antigen 6 recognized by MAb-6, showed significantly lower adherence ability to all the human epithelial cell lines used than did C. albicans A, which bears antigen 6. These results suggest that so far as mannan side chain is concerned, serotype A-specific antigen 6 in the mannan plays a significant role in adherence to various types of human epithelial cells.

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We developed an enzyme immunoassay system (EIA-1) to compare its sensitivity and specificity with those of a commercially available EIA kit (EIA-2) and with a latex agglutination (LA) kit prepared in our laboratory. When antigens were diluted with buffer, the minimal detectable concentration of polysaccharide antigens from Cryptococcus neoformans serotypes A and B was 0.10ng/ml and 0.05ng/ml, respectively. The EIA-1 was found to be 32-fold more sensitive than EIA-2, and 64-fold (for serotype A) and 256-fold (for serotype B) more sensitive than the LA test. Cross-reactivity with Candida albicans and Aspergillus fumigatus antigens was not observed with either EIA, nor did rheumatoid factor give a false-positive reaction. However, when capsular polysaccharides were diluted with human serum, the sensitivity of both EIAs decreased. With sera from patients, although sensitivity of the EIA-2 test was similar to that of the LA test, EIA-1 exhibited lower antigen titers than did the other two tests. It was suggested that EIA using monoclonal antibodies is affected by serum condition. Taken together, because of its sensitivity, specificity, ease of performance, reproducibility and rapidity, except for a pretreatment procedure for rheumatoid factor, the LA test would be the most useful for serodiagnosis of cryptococcosis.

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We report a rare case of allergic bronchopulmonary aspergillosis (ABPA) with pulmonary atelectasis and free of asthmatic symptoms.
A 65-year-old female was admitted to Sawara Hospital on October 28, 1992 because of a dry cough. At the time of admission, phisical examination revealed no abnormal findings. Laboratory examinations showed only a peripheral eosinophilia, and the chest X-ray film showed an infiltration shadow in the left upper lobe. The patient was treated with 400mg/day of clarithromycin for 8 days, but no clinical improvement was seen. In addition, the chest X-ray film showed pulmonary atelectasis in the left upper lobe. Initial broncho-fiberscopy examination revealed whitish-yellow spots on the wall of the left upper bronchus. Aspergillus fumigatus was isolated from the biopsy specimen. Total IgE and specific IgE measured by a RAST test were elevated to 15, 130IU/ml and 22.8UA/ml, respectively. The precipitating antibody against aspergillus antigen was positive.
The patient was then treated and cured with a clearance of the broncho-obliteration, and with a daily dose of fluconazole (FLCZ) 400mg for 40 days. The early elimination of the broncho-obliteration was more effective because the MIC of FLCZ was 100μg/ml.

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The agar implantation method allows observation of the parasitic form of a fungus by intraperitoneally implanting agar blocks inoculated with the fungus into mice. In the present study, we adapted this method by implanting agar blocks intradermally in mice to observe transepidermal elimination in chromomycosis. Agar blocks containing the fungal elements of Foncecaea pedrosoi were implanted intradermally into the backs of C57BL/6 mice, and the areas of skin including the agar blocks were sequentially harvested and examined histologically. Infiltration of polymorphonuclear leukocytes and lymphocytes was seen around the agar blocks at 2 weeks after implantation. After 4 weeks, histiocytes and epithelioid cells appeared and a pyogenic granuloma formed. At the same time, pseudocarcinomatous hyperplasia of the epidermal processes overlying the agar block was seen. From 6 weeks onwards, the epidermal processes which surrounded the infiltrating cells became longer, and microabscesses partially surrounded by these elongated processes were noted as well as transepidermal elimination of agar containing hyphae. These results suggest that intradermal agar implantation is a useful method for the sequential observation of early infection and transepidermal elimination in chromomycosis.

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The chronological history of the development of our knowledge concerning superficial mycoses and their etiologic agents is presented. These are: pityriasis versicolor-Malassezia furfur; white piedra-Trichosporon beigelii; pityriasis nigra-Phaeoannellomyces werneckii, Stenella araguata, and black piedra-Piedraia hortai. The potential for M. furfur, M. pachydermatis and T. beigelii to induce life threatening systemic infections-malasseziasis furfurii, malasezziasis pachydermatisii and trichosporonosis beigelii-is also discussed.

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